Reactive oxygen species and tendon problems: Review and hypothesis

Abstract

The biochemical mechanisms underlying exercise-related tendon damage and predisposition to repetitive injury are obscure, and there is little information available within the current literature. However, exercise is associated with elevated production of reactive oxygen species. Such species are traditionally viewed as inducers of cellular or tissue damage, but it is now apparent that reactive oxygen (in cooperation or antagonism with reactive nitrogen species) at sublethal levels mediates processes as diverse as proliferation, differentiation, and adaptation. We review evidence to suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and also from the tenocytes themselves, the latter, possibly, as a response to hyperthermia and during repetitive ischemia or reperfusion. We subsequently extend an hypothesis of how such species may influence the development of tendinopathies.

title = "Reactive oxygen species and tendon problems: Review and hypothesis",

abstract = "The biochemical mechanisms underlying exercise-related tendon damage and predisposition to repetitive injury are obscure, and there is little information available within the current literature. However, exercise is associated with elevated production of reactive oxygen species. Such species are traditionally viewed as inducers of cellular or tissue damage, but it is now apparent that reactive oxygen (in cooperation or antagonism with reactive nitrogen species) at sublethal levels mediates processes as diverse as proliferation, differentiation, and adaptation. We review evidence to suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and also from the tenocytes themselves, the latter, possibly, as a response to hyperthermia and during repetitive ischemia or reperfusion. We subsequently extend an hypothesis of how such species may influence the development of tendinopathies.",

N2 - The biochemical mechanisms underlying exercise-related tendon damage and predisposition to repetitive injury are obscure, and there is little information available within the current literature. However, exercise is associated with elevated production of reactive oxygen species. Such species are traditionally viewed as inducers of cellular or tissue damage, but it is now apparent that reactive oxygen (in cooperation or antagonism with reactive nitrogen species) at sublethal levels mediates processes as diverse as proliferation, differentiation, and adaptation. We review evidence to suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and also from the tenocytes themselves, the latter, possibly, as a response to hyperthermia and during repetitive ischemia or reperfusion. We subsequently extend an hypothesis of how such species may influence the development of tendinopathies.

AB - The biochemical mechanisms underlying exercise-related tendon damage and predisposition to repetitive injury are obscure, and there is little information available within the current literature. However, exercise is associated with elevated production of reactive oxygen species. Such species are traditionally viewed as inducers of cellular or tissue damage, but it is now apparent that reactive oxygen (in cooperation or antagonism with reactive nitrogen species) at sublethal levels mediates processes as diverse as proliferation, differentiation, and adaptation. We review evidence to suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and also from the tenocytes themselves, the latter, possibly, as a response to hyperthermia and during repetitive ischemia or reperfusion. We subsequently extend an hypothesis of how such species may influence the development of tendinopathies.